Chinese Journal of Tissue Engineering Research ›› 2013, Vol. 17 ›› Issue (11): 1959-1964.doi: 10.3969/j.issn.2095-4344.2013.11.009

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Integrin beta 1 inhibits long-term potentiation induced by amyloid beta-protein

Han Hai-yan1, Zhang Yi-chi2, Ji Shu-qiong1, Liang Qi-ming1, Zhu Sui-qiang1, Xue Zheng1   

  1. 1 Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China
    2 Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China
  • Received:2012-06-06 Revised:2012-07-24 Online:2013-03-12 Published:2013-03-12
  • Contact: Xue Zheng, M.D., Associate professor, Associate chief physician, Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China xuezheng@tjh.tjmu.edu.cn
  • About author:Han Hai-yan★, Master, Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Province, China zhicgub16@163.com

Abstract:

BACKGROUND: Inhibition of integrin activity in the hippocampal slices of mice cannot influence the induction of long-term potentiation, but bring rapid long-term potentiation attenuation, proving integrin plays a key role in maintaining and stabilizing the long-term potentiation after induction.
OBJECTIVE: To explain the influence of integrin beta-1 subunit during the inhibition of long-term potentiation induced by amyloid beta-protein in rat hippocampus CA1 in vivo using electrophysiological technology.
METHODS: Fifteen Sprague-Dawley rats were equally randomized into control group treated with normal saline, amyloid beta-protein group treated with amyloid beta-protein, and integrin beta-1 subunit inhibitor group treated with selective antagonist for integrin beta-1 subunit. Excitatory postsynaptic potentials were recorded from 10 minutes before amyloid beta-protein administration till 3 hours after high-frequency tetanic stimulation.
RESULTS AND CONCLUSION: In the control group, excitatory postsynaptic potentials were enhanced significantly with an increment of 30%. In the amyloid beta-protein group, excitatory postsynaptic potentials were obviously restraint within 3 hours after high-frequency tetanic stimulation and had no remarkable increase. It can be speculated by the results that integrin beta-1 subunit may be important to the long-term potentiation inhibited by amyloid beta-protein in the rat hippocampal CA1 region in vivo. The special inhibitor or antibody of integrin beta-1 subunit has the ability to stop the mediation.

Key words: tissue construction, tissue construction and bioactive factors, Alzheimer’s disease, neurotoxicity, amyloid beta-protein, long-term potentiation, integrin beta-1 subunit, hippocampal CA1 region, high-frequency stimulation, excitatory postsynaptic potential, the National Natural Science Foundation of China, tissue construction photographs-containing paper

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